Pressure ulcers represent a very significant cost burden in the UK. Without concerted effort this cost is likely to increase in the future as the population ages. To the extent that pressure ulcers are avoidable, pressure damage may be indicative of clinical negligence and there is evidence that litigation could soon become a significant threat to healthcare providers in the UK, as it is in the USA.
OBJECTIVE The purpose of this trial was to compare usual patient education plus the Internet-based, Personal Patient Profile-Prostate, versus usual education alone, on conflict associated with decision making, plus explore time-to-treatment and treatment choice. METHODS A randomized, multi-center clinical trial was conducted with measures at baseline, one and six months. Men with newly diagnosed localized prostate cancer who sought consultation at urology, radiation oncology or multi-disciplinary clinics in four geographically-distinct American cities were recruited. Intervention group participants used the Personal Patient Profile-Prostate, a decision support system comprised of customized text and video coaching regarding potential outcomes, influential factors, and communication with care providers. The primary outcome, patient-reported decisional conflict, was evaluated over time using Generalized Estimating Equations to fit generalized linear models. Additional outcomes, time-to-treatment, treatment choice and program acceptability/usefulness, were explored. RESULTS A total of 494 eligible men were randomized (266 intervention; 228 control). The intervention reduced adjusted decisional conflict over time as compared with the control group, for the uncertainty score (estimate −3.61; (confidence interval, −7.01,−0.22) and values clarity (estimate −3.57; confidence interval (−5.85,−1.30) Borderline effect was seen for the total decisional conflict score (estimate −1.75; confidence interval (−3.61,0.11). Time-to-treatment was comparable between groups, while undecided men in the intervention group chose brachytherapy more often than in the control group. Acceptability and usefulness were highly rated. CONCLUSION The Personal Patient Profile-Prostate is the first intervention to significantly reduce decisional conflict in a multi-center trial of American men with newly diagnosed localized prostate cancer. Our findings support efficacy of P3P for addressing decision uncertainty and facilitating patient selection of a prostate cancer treatment that is consistent with the patient values and preferences.
Chemotherapy-associated memory deficits in adults are prevalent with systemic treatment utilizing 5-fluorouracil (5-Fu). 5-Fu disrupts cell proliferation and readily crosses the blood-brain barrier. Proliferating cells within the adult dentate gyrus of the hippocampus give rise to new neurons involved in memory and learning and require neurotrophic factors such as brain-derived neurotrophic factor (BDNF) to nurture this process of adult neurogenesis. Some of these proliferating cells are anatomically and functionally supported by vascular endothelial cells. We propose that systemically administered 5-Fu chemotherapy will cause deficits in hippocampal memory that are associated with altered BDNF levels and proliferating cells (particularly vascular-associated cells) in the dentate gyrus. This was tested by determining the effect of 5-Fu on spatial working memory as modelled by the object location recognition test. Numbers of vascular-associated (VA) and non-vascular-associated (NVA) proliferating cells in the dentate gyrus were measured using double-labelling immunohistochemistry with markers of proliferation (Ki67) and endothelial cells (RECA-1). 5-Fu-induced changes in hippocampal BDNF and doublecortin (DCX) protein levels were quantified using Western immunoblotting. 5-Fu chemotherapy caused a marginal disruption in spatial working memory and did not alter the total proliferating cell counts or the percentage of VA and NVA proliferating cells in the dentate gyrus. In contrast, 5-Fu significantly reduced BDNF and DCX levels in the hippocampus, indicating alterations in neurotrophin levels and neurogenesis. These findings highlight the usefulness of animal models of 'chemobrain' for understanding the mechanisms that underlie chemotherapy-associated declines in cognitive performance and memory.
There has been a recent surge of interest in
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